In addition, another research demonstrated that silencing IGF1R expression through employing a CRISPR/Cas9 genome editing system leads to functional endpoint mechanism for TKI resistance in a targetable direction MET-amplification, and thereby resulting in improving response to treatment via suppressing resistance to Erlotinib in Non-Small Cell Lung Carcinoma cells and inhibiting epithelial-mesenchymal transition in tumor cells (Hussmann et al., 2017). This evidence concerns the gene IGF1R and neoplasm.